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Biomedical subjects

A J Larner

Publications and source records attributed to A J Larner.

At least 91 records · Page 5Linked to original sources
PubMed1999

Bilateral symmetrical enhancing brainstem lesions: an unusual presentation of primary CNS lymphoma.

We report a patient with a progressive brainstem syndrome, who on magnetic resonance imaging had large bilateral, symmetrical, contrast-enhancing, infratentorial space-occupying lesions. Biopsy of one of the lesions revealed this unusual appearance to be due to a primary central nervous system (CNS) lymphoma of B-cell type. Symmetry of lesions may be a clue to the diagnosis, perhaps reflecting the mechanism by which CNS lymphomas spread.

Aged↗
PubMed1999

Spatz-Lindenberg disease: a rare cause of vascular dementia.

BACKGROUND: Isolated cerebral thromboangiitis obliterans (Spatz-Lindenberg disease) is not well recognized as a cause of vascular dementia. CASE DESCRIPTION: A 58-year-old woman presented with dementia and pyramidal signs. Neuroimaging showed multiple areas of white matter change. Brain biopsy showed intimal thickening of the walls of leptomeningeal and intraparenchymal arteries, almost to complete occlusion, with an intact internal elastic lamina and media and without inflammation or infiltration. The cortex showed only moderate gliosis. CONCLUSIONS: Spatz-Lindenberg disease should be considered in the differential diagnosis of vascular dementia. Additional studies of its pathogenesis are required to determine appropriate treatment.

Cerebrovascular Disorders↗
PubMed1998

Complex partial status epilepticus in late-onset MELAS.

A patient with recurrent episodes of complex partial status epilepticus and a distinctive pattern of periodic lateralized epileptiform discharges (PLEDs) is presented. The patient was subsequently shown to have a mitochondrial disorder of the MELAS type, a hitherto unreported association. The case illustrates that CPSE should be added to the list of possible causes of acute neurological deterioration in MELAS patients.

Diagnosis, Differential↗
PubMed1998

Upbeat nystagmus: clinicoanatomical correlation.

A patient is reported on with isolated upbeating nystagmus with a linear slow phase in whom a solitary lesion, probably inflammatory, was detected radiologically in the dorsal paramedian caudal medulla, encompassing the most caudal of the perihypoglossal nuclei, the nucleus intercalatus of Staderini. The conjunction of a vestibular pattern of nystagmus with this focal lesion runs contrary to a previous suggestion that the nucleus intercalatus may act as a neural integrator for vertical conjugate eye movements.

Adult↗
PubMed1998

Myasthenic hand.

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Aged↗
PubMed1996

Smallpox.

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Anniversaries and Special Events↗
PubMed1996

Alzheimer's disease, Kuf's disease, tellurium and selenium.

The possible role of the abnormal trace element tellurium in the pathogenesis of Alzheimer's disease is examined. Tellurium has been reported to produce cognitive impairment and cerebral lipofuscinosis in rats-changes akin to those seen in Kuf's disease, a condition which shares certain clinical and neuropathological features with Alzheimer's disease. Tellurium can damage mitochondria; defects in mitochondrial energy metabolism may be relevant to the pathogenesis of neurodegenerative disease. The deficiency of selenium, which may act physiologically as an antagonist of tellurium, in the Alzheimer's disease brain would also be in keeping with the hypothesis of tellurium toxicity as a factor in the pathogenesis of Alzheimer's disease.

Adult↗
PubMed1996

Focal upper limb demyelinating neuropathy.

Observations are presented on nine selected patients with chronic upper limb demyelinating neuropathy to illustrate the range of manifestations that may be observed. In three, the involvement was purely motor, in five, mixed motor and sensory and, in one, virtually purely sensory; in seven the symptoms were unilateral and in two bilateral. The presence of reduced nerve conduction velocity and conduction block and the response to treatment in seven of the cases indicate that they represented examples of chronic inflammatory demyelinating polyneuropathy (CIDP) with focal involvement. This was confirmed by nerve biopsy in two cases. The presentation in one patient was accompanied by forearm swelling initially suspected of being a tumour but shown to be due to muscle hypertrophy. This was probably the consequence of recurrent muscle cramps and fasciculation and possibly neuromyotonia. The patient with predominant sensory involvement restricted to the upper limbs demonstrates that sensory CIDP can present focally. In one patient with monomelic motor and sensory involvement, nerve biopsy showed multifocal areas of hypertrophic demyelinating neuropathy distally in the ulnar nerve without inflammatory infiltration. This patient failed to respond to therapy. Response in the others was satisfactory, although one patient with a monomelic motor neuropathy showed a severe deterioration after being given corticosteroids; he subsequently improved with intravenous human immunoglobulin therapy.

Adolescent↗
PubMed1995

Physiological and pathological interrelationships of amyloid beta peptide and the amyloid precursor protein.

Amyloid beta peptide (beta A4) accumulates as plaques in the brains of individuals with Alzheimer's disease and Down's syndrome, and may contribute to the cognitive decline that is a feature of these diseases. beta A4 is a normal product of cell metabolism, derived from the amyloid precursor protein (APP), but the biological functions of these molecules are not fully known. A hypothetical, descriptive model of the biological interrelationships between beta A4 and APP is presented. APPs, the soluble form of APP, which is released at the neuronal surface, and beta A4 are envisaged as physiological ligands which have reciprocal paracrine effects on neuronal growth and neurite extension. Differential expression of these factors, manifest as changes in the APPs: beta A4 ratio, may therefore have growth-promoting or growth-inhibiting effects on neurons. These effects may be mediated through separate cell-surface interactions but common intracellular effector systems, such as calcium and protein kinase C. In turn, the intracellular events may control the relative production of each ligand from APP through negative feedback loops. Disturbances of these control mechanisms may permit pathological overproduction, and hence accumulation, of beta A4. Such a model may also have therapeutic implications.

Adult↗